Alexa Storozuk represented Manitoba at the 2026 Canada-Wide Science Fair
A West St. Paul student is helping advance research into a rare neurological disorder through a complex science project that examines how brain cells communicate and what happens when that communication breaks down.
Alexa Storozuk represented Manitoba at the 2026 Canada-Wide Science Fair in Edmonton with her project, “Investigating the Mechanisms of ELFN1 Deficiency Disorder.”
The national competition, organized by Youth Science Canada, brought together nearly 400 of Canada’s top student researchers from May 23 to 30 at the Edmonton EXPO Centre and the University of Alberta. Students competed for more than $2 million in scholarships, awards and prizes while showcasing projects in science, technology, engineering and mathematics.
Storozuk’s research focused on ELFN1 Deficiency Disorder, a rare neurodevelopmental genetic condition linked to symptoms including ADHD, autism spectrum disorder, epilepsy, seizures and developmental delays.
“Our brains require proper neuronal cell communication to work,” Storozuk explained in her project summary.
She studied how a protein called ELFN1 helps neurons communicate at the synapse — the connection point between nerve cells in the brain. The protein binds to a glutamate receptor that helps regulate glutamate, a chemical messenger involved in stimulating brain activity.
When the communication process is disrupted, it can lead to neurological disorders.
For her project, Storozuk examined two specific genetic variants of the ELFN1 protein to better understand how the disorder develops and affects brain function.
“As it is a newly identified condition, there are currently gaps in our literature and understanding of it,” she noted. “My research aims to build foundational knowledge of the pathogenic and molecular function of this disorder.”
Her findings showed the two variants behave differently within the brain’s communication system.
One variant appeared unable to function properly because it showed reduced membrane expression and difficulty regulating receptor signalling. The second variant still appeared to function normally in some ways, suggesting it may instead disrupt signalling pathways inside the synapse and contribute to epilepsy and seizures.
Storozuk said understanding these mechanisms could help researchers eventually develop therapies or treatments for patients living with the disorder.
She also explored the potential use of positive allosteric modulators (PAMs), a type of drug that has previously improved symptoms in mice lacking the ELFN1 protein.
“Such strategies may offer a promising approach for symptom reduction and improved quality of life,” she stated in her conclusion.
The project remains ongoing research, with Storozuk planning additional laboratory testing to further study how ELFN1 variants interact with brain receptors and function within cells.
Her future plans include advanced cell studies using stem cells reprogrammed from patient blood cells, as well as research involving mouse models to better understand the disorder and evaluate potential treatments.
